Evidence has accumulated in both human and animal studies to suggest a common secretory immune system. Such data suggest selective homing of IgA lymphoblasts from the gastrointestinal tract and other secretory sites to the mammary gland. Human studies with antigen-induced lymphocyte blastogenesis have led to the proposal that breast milk T lymphocytes may also represent a select lymphocyte population different from that in the peripheral blood. Lymphocytes reactive to certain antigens (Candida albicans, streptokinase/streptodornase, and tetanus toxoid) were reported to be absent from milk while lymphocytes reactive to the Kl antigen of E. coli were selectively present in milk yet absent from blood. My own data with Kl antigen and streptokinase/ streptodornase antigen (using T cell enriched, macrophage depleted lymphocyte preparations) conflict with the results from these earlier studies, but further extension is needed with Candida antigen to support my hypothesis that the T cell population of milk is similar to the T cell population of the peripheral blood. Lymphokine production by milk lymphocytes has not been thoroughly studied although transfer of cellular immunity from human breast milk to suckling neonates could be modulated through absorption of lymphokines. This project will study immune interferon and lymphocyte derived chemotactic factor production by milk and blood lymphocytes to further characterize the milk lymphocyte population. Finally, this project will determine if breast milk can transfer cellular immunity to Herpes simplex type 1 antigen from the mother to the infant by comparing lymphocyte blastogenesis to this antigen in breast fed and bottle fed infants.